Evidence map›Paper›PMID 37041551›Full record

ArticleFluids and barriers of the CNS2023

Movement of cerebrospinal fluid tracer into brain parenchyma and outflow to nasal mucosa is reduced at 24 h but not 2 weeks post-stroke in mice.

K E Warren, K G Coupland, R J Hood, L Kang, F R Walker, N J Spratt

Open access · goldAbstract read
In one paragraph

Article in Fluids and barriers of the CNS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 38% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Intracranial pressure is elevated at 24 h post-stroke in mice.Neuroprotection (Chichester, England) · 2024
    Article
  6. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

K E WarrenSchool of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan and Hunter Medical Research Institute, University Drive, Callaghan, New Lambton Heights, NSW, 2308, Australia.
K G CouplandSchool of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan and Hunter Medical Research Institute, University Drive, Callaghan, New Lambton Heights, NSW, 2308, Australia.
R J HoodSchool of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan and Hunter Medical Research Institute, University Drive, Callaghan, New Lambton Heights, NSW, 2308, Australia.
L KangSchool of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan and Hunter Medical Research Institute, University Drive, Callaghan, New Lambton Heights, NSW, 2308, Australia.
F R WalkerSchool of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan and Hunter Medical Research Institute, University Drive, Callaghan, New Lambton Heights, NSW, 2308, Australia.
N J SprattSchool of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan and Hunter Medical Research Institute, University Drive, Callaghan, New Lambton Heights, NSW, 2308, Australia. Neil.Spratt@health.nsw.gov.au.
Hunter Medical Research Institute · AUUniversity of Newcastle Australia · AUHunter New England Local Health District · AU

Funding

National Health and Medical Research Council G1700230National Health and Medical Research Council GNT1110629National Heart Foundation of Australia 100827
6 · The paper itself

Abstract

backgroundRecent data indicates that cerebrospinal fluid (CSF) dynamics are disturbed after stroke. Our lab has previously shown that intracranial pressure rises dramatically 24 h after experimental stroke and that this reduces blood flow to ischaemic tissue. CSF outflow resistance is increased at this time point. We hypothesised that reduced transit of CSF through brain parenchyma and reduced outflow of CSF via the cribriform plate at 24 h after stroke may contribute to the previously identified post-stroke intracranial pressure elevation.

methodsUsing a photothrombotic permanent occlusion model of stroke in C57BL/6 adult male mice, we examined the movement of an intracisternally infused 0.5% Texas Red dextran throughout the brain and measured tracer efflux into the nasal mucosa via the cribriform plate at 24 h or two weeks after stroke. Brain tissue and nasal mucosa were collected ex vivo and imaged using fluorescent microscopy to determine the change in CSF tracer intensity in these tissues.

resultsAt 24 h after stroke, we found that CSF tracer load was significantly reduced in brain tissue from stroke animals in both the ipsilateral and contralateral hemispheres when compared to sham. CSF tracer load was also reduced in the lateral region of the ipsilateral hemisphere when compared to the contralateral hemisphere in stroke brains. In addition, we identified an 81% reduction in CSF tracer load in the nasal mucosa in stroke animals compared to sham. These alterations to the movement of CSF-borne tracer were not present at two weeks after stroke.

conclusionsOur data indicates that influx of CSF into the brain tissue and efflux via the cribriform plate are reduced 24 h after stroke. This may contribute to reported increases in intracranial pressure at 24 h after stroke and thus worsen stroke outcomes.

Indexed as

BrainStrokeAnimalsIntracranial PressureMaleMiceMice, Inbred C57BLNasal MucosaCerebrospinal fluidCribriform plateIntracranial pressureIschaemic strokeStroke

Identifiers

PMID37041551
PMCPMC10088200
OpenAlexW4364365852

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.